The cellular character of liquefaction degeneration in oral lichen planus and the role of interferon gamma

Liu, Yuan; Liu, Guicai; Liu, Qing; Tan, Jun; Hu, Xin; Wang, Jinjin; Wang, Qintao; Wang, Xinwen

doi:10.1111/jop.12595

Cited by 19 publications

(20 citation statements)

References 32 publications

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“…Increased SOCS1 mRNA levels correlated with increased IL-10 expression levels in periapical granuloma [48], and with phosphorylated STAT1 expression levels in ligature-induced periodontitis in rats [49]. Furthermore, the expression of phosphorylated STAT1 is allowed in immunostaining of OLP [50]. In this study, increase of SOCS1 mRNA expression levels in OLP may be related closely to the activation of STAT1…”

Section: Discussionsupporting

confidence: 53%

Methylation and Expression Status of SOCS1 and SOCS3 in Oral Lichen Planus

Yoshimura¹,

Yada²,

Matsuo³

et al. 2018

OJST

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Oral lichen planus (OLP) is a disease of unknown etiology affecting oral mucosa by mediated chronic inflammation and is classified as a potentially malignant oral disorder. SOCS1 and SOCS3 in the SOCS family have been identified as negative regulators of the cytokine-activated JAK/STAT pathway responsible for inflammatory reaction. The DNA methylation in the promoter regions of SOCS1 and SOCS3 have been reported to correlate with carcinogenesis. In this study, we performed methylation-specific PCR (MSP) to investigate the methylation status of the promoter regions in SOCS1 and SOCS3 genes using biopsy samples from OLP and oral squamous cell carcinoma (OSCC) patients. SOCS1 was methylated in 14/29 (48.3%) cases with OLP and 7/15 (46.7%) cases with OSCC. At the same time, SOCS3 was methylated in 25/29 (86.2%) cases with OLP and 11/15 (73.3%) cases with OSCC. We didn't recognize any DNA methylation in SOCS1 or SOCS3 genes from the exfoliated cytological specimens of normal buccal mucosa. Furthermore, mRNA expression level was analyzed using real-time RT-PCR method to evaluate the correlation with DNA methylation status. DNA methylation status of SOCS1 seemed not to affect the expression level of SOCS1 mRNA. At the same time, DNA methylation status of SOCS3 was negatively correlated with the expression level of SOCS3 mRNA (p < 0.05). We posit frequent methylation of the SOCS3 gene promoter, theoretically resulting in the increase of cytokines expression, might be associated with the etiological mechanism of OLP.

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Section: Discussionsupporting

confidence: 53%

Methylation and Expression Status of SOCS1 and SOCS3 in Oral Lichen Planus

Yoshimura¹,

Yada²,

Matsuo³

et al. 2018

OJST

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“…Previous investigations have shown that epithelial expression of keratins is altered in OLP compared with normal oral mucosa and this can therefore affect the functions mentioned above: keratin 1 (K1)/keratin 10 (K10) , K14 , keratin 6 (K6)/keratin 16 (K16), and K19 are reported to be upregulated in OLP, whereas keratin 4 (K4) , K4/keratin 13 (K13) , keratin 5 (K5)/keratin 15 (K15) , and K19 are reported to be downregulated. Data on K8 and K18 expression in oral keratinocytes of normal oral mucosa are inconsistent, varying from reports of absence to sporadic presence .…”

mentioning

confidence: 99%

Expression of keratins 8, 18, and 19 in epithelia of atrophic oral lichen planus

Schreurs

Karatsaidis

Balta

et al. 2020

European J Oral Sciences

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Keratins form intermediate filaments of the cytoskeleton in keratinocytes and have roles in cell structure, signaling, intracellular transport, and cell death. Oral lichen planus (OLP) is an oral inflammatory disease with derangements in basal keratinocytes and disruption of the basal membrane. Here, we focused on epithelial expression of keratins 8, 18, and 19 because these proteins are known to modulate cell death. Biopsies were taken from buccal oral mucosa of persons with normal oral mucosa (n = 10) or atrophic OLP (n = 10). Cultured normal oral keratinocytes (n = 4) showed expression of mRNA and protein for keratins 8, 18, and 19. Immunohistochemistry showed consistent staining for keratins 8 and 18 in basal keratinocytes of normal oral mucosa. In OLP, staining for keratin (K)8 was mostly negative and staining for K18 was weak. Keratin 19 was expressed irregularly in most biopsies of normal oral mucosa and not at all in OLP. Several mononuclear leukocytes in the cellular infiltrate showed membrane staining for K8 and K18. Positive staining for K16 confirmed partial collapse of the basal cell layer in OLP. The basal cell niche in OLP therefore appeared to be partly populated with keratinocytes demonstrating a higher degree of differentiation (K8− K18− K19− K16+); consequently, such areas may be more susceptible to the action of cell death factors released from the cell infiltrate as a result of lacking the protective, normal keratin present in the basal epithelial cell layer of normal oral mucosa.

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“…On the contrary, IFNγ directly induces morphological changes in epithelial cells from polygonal shape to fibroblast-like shape, loss of cell-to-cell contact, E-cadherin overexpression and downregulated Vimentin expression, which finally results in the liquefactive degeneration of basal keratinocytes in OLP. 34 Additionally, IFNγ-inducible CCL27 secretion from keratinocytes is involving in the recruitment of memory T cells into epithelium, which might be associated with the recurrence and chronicity of OLP. 35 In the present study, keratinocytes that were co-cultured with OLP-derived T cells had a larger number of apoptotic populations than ones cultured alone.…”

Section: -Dg Is Considered As An Inhibitor Of Glucose Metabolismmentioning

confidence: 99%

2‐Deoxy‐D‐glucose impedes T cell–induced apoptosis of keratinocytes in oral lichen planus

Wang

Zhang

Zhou

2021

J Cellular Molecular Medi

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Oral lichen planus (OLP) is a chronic inflammatory immune disease of unknown aetiology and has been recognized as an oral potentially malignant disorder (OPMD). 1,2 The typically histopathological characteristics of OLP are dense subepithelial infiltration of lymphocytes and liquefactive degeneration in the basal keratinocytes. 2 T cell-mediated dysfunctional immunity has been widely supposed to be the main pathogenesis of OLP. 3,4 Our previous studies demonstrated that Th1-biased responses participated in the development of OLP. 5,6 Specifically, T helper (Th) cells are activated after antigen presentation by major histocompatibility complex II (MHC-II) molecules and then produce pro-inflammatory cytokines, including interferonγ (IFNγ) and interleukin-2 (IL-2). 4 These cytokines together with MHC-I molecules on keratinocytes activate cytotoxic T cells, which further induce the apoptosis of keratinocytes. 4 The metabolic reprogramming in T-cell immune responses is characterized by a switch to aerobic glycolysis, also known as 'Warburg effect' that was first described in cancer. 7 Blocking aerobic glycolysis is pernicious to proliferation and differentiation of effector T cells

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The cellular character of liquefaction degeneration in oral lichen planus and the role of interferon gamma

Abstract: Liquefaction degeneration in oral lichen planus is an EMT phenomenon, the IFN-γ may be the main inducer, and IFN-γ signaling might be implicated in malignant transition of OLP.

Cited by 19 publications

References 32 publications

Methylation and Expression Status of <i>SOCS</i>1 and <i>SOCS</i>3 in Oral Lichen Planus

Methylation and Expression Status of <i>SOCS</i>1 and <i>SOCS</i>3 in Oral Lichen Planus

Expression of keratins 8, 18, and 19 in epithelia of atrophic oral lichen planus

2‐Deoxy‐D‐glucose impedes T cell–induced apoptosis of keratinocytes in oral lichen planus

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The cellular character of liquefaction degeneration in oral lichen planus and the role of interferon gamma

Abstract: Liquefaction degeneration in oral lichen planus is an EMT phenomenon, the IFN-γ may be the main inducer, and IFN-γ signaling might be implicated in malignant transition of OLP.

Cited by 19 publications

References 32 publications

Methylation and Expression Status of &lt;i&gt;SOCS&lt;/i&gt;1 and &lt;i&gt;SOCS&lt;/i&gt;3 in Oral Lichen Planus

Methylation and Expression Status of &lt;i&gt;SOCS&lt;/i&gt;1 and &lt;i&gt;SOCS&lt;/i&gt;3 in Oral Lichen Planus

Expression of keratins 8, 18, and 19 in epithelia of atrophic oral lichen planus

2‐Deoxy‐D‐glucose impedes T cell–induced apoptosis of keratinocytes in oral lichen planus

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Methylation and Expression Status of <i>SOCS</i>1 and <i>SOCS</i>3 in Oral Lichen Planus

Methylation and Expression Status of <i>SOCS</i>1 and <i>SOCS</i>3 in Oral Lichen Planus